Abstract

Cold sores produced by HSV-1 infection are an annoying but trivial recurrent problem for most of us, but the virus can also cause more serious disease. Episodes of active HSV-1 infection, in response to stress or sunlight, are possible because the virus establishes a latent infection in neurones which can not be eliminated. Since vigorous transcription from the whole viral genome during lytic infection contrasts with almost complete quiescence during latency, the mechanisms controlling HSV-1 gene expression have come under close scrutiny. These studies have demonstrated that the viral immediate-early protein ICP0, a promiscuous activator of gene expression, is required for efficient initiation of lytic infection and reactivation from latency. It is proposed that in the absence of functional ICP0, a cellular repression mechanism silences viral transcription. ICP0 appears to counteract this process by stimulating the degradation of a number of cellular proteins via the ubiquitin-proteasome pathway.

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